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Functional Ess

Functional ESS, which espouses a more limited approach, can and should be used whenever the disease process dictates its appropriateness. Smith and Brindley, utilizing this approach, found comparable results when compared with studies using more extensive interventions. Experience of the surgeon, as alluded to earlier, plays a large part in determining the risk of an adverse outcome.

Finally, familiarity with endoscopic anatomy and its variations play an extremely important part in reducing complications. As in all of surgery, anatomical landmarks are critical to maintaining spatial orientation. This is also true in the nasal cavity. The close proximity of the ethmoid sinuses to the skull base and brain as well as the orbit and optic nerve mandates continuous awareness of one’s location. Streitmann et al studied 50 cadaveric heads and performed several measurements from the base of the columella to various important landmarks, relating both the angle of incidence and the distance to these structures.

Ohnishi identified 5 high-risk areas that he considered to merit special attention during ESS. The lamina papyracea, given its protrusion into the field and its relative fragility, is an area that is frequently violated. Injury in this area predisposes to medial rectus entrapment or transection. Extensive manipulation in this region has resulted in blindness in some cases. The anterior ethmoid artery and roof are likewise in a susceptible location, and injury laterally can predispose to either significant hemorrhage into the field or to orbital hematoma if the vessel retracts in its bony canal. Injury more medially, with fracture of the attenuated ethmoid roof, is a common cause for CSF leak and predisposes to possible meningitis. The lateral lamella of the cribriform plate (also the lateral wall of the olfactory bulb) is an area where attempts at complete exenteration of superior ethmoid air cells can result in small dehiscences that predispose to an increased risk of infection. The posterior ethmoid roof and artery, although usually not problematic, may present with a dehiscent artery lying inferior to the roof, with or without a bony canal. Finally, the area Between the posterior ethmoid and the sphenoid sinus is of critical significance because it is here where anatomical variations can predispose to inadvertent injury to the optic nerve or the carotid artery. Takedown of thick bony buttresses in this area should not be performed as fracture planes can be created that run into the carotid artery bony canal with possible pseudoaneurysm formation or fistulization to the cavernous sinus.

As important as familiarity with normal anatomy is, it is of equal importance to be aware of the anatomical variants that one might encounter in performing ESS. Bolger, in a detailed analysis of 202 consecutively-imaged patients, identified several bony anatomic variations. The most common of these, the agger nasi, which was present in 98.5% of patients, is described as being the most anterior of the anterior ethmoid cells, bounded superiorly by the frontal sinus. These can be quite large, may displace the lamina papyracea to a more lateral position. A concha bullosa (or pneumatized middle turbinate) was present in 53% of cases. No consistent relationship between the presence of this variation and the pathogenesis of OMC disease has been established. The need for resection of these should proceed on a patient-to-patient basis, as these may be the reason for primary disease at the OMC.

Haller’s Cells are ethmoid cells that project into the maxillary sinus. Although it was present in 45% of scans, not all Haller cells are pathologically important. Again, case-by-case evaluation of these entities is required to assess their role in contributing to maxillary ostium blockage.

The Onodi Cell is a posterior ethmoid cell that has encroached upon the area of the sphenoid sinus. It is of considerable significance because in a large majority of these, a frankly dehiscent optic nerve, carotid artery or both may be present in variable locations. Several other variants have been described.

Among these are the uncinate bulla, which although relatively infrequent, may alter the anatomy at the OMC. Others include Bulla Gali (5.4%), pterygoid pneumatization (43.6%), and anterior clinoid pneumatization (13.3%). Preoperative recognition of these variations is useful as these at times may require special attention in order to prevent postoperative recurrent disease, and more importantly, complications by allowing the surgeon to better estimate the limits of resection.

I would now like to discuss the prevention and management three complications, that, if detected early, can be dealt with before more severe delayed sequelae evolve. These include massive hemorrhage, cerebrospinal fluid leak, and orbital hematoma. The management of synechiae and of nasolacrimal duct obstruction will also be briefly reviewed.

Massive hemorrhage, resulting from major vascular injury, is an exceedingly rare complication. Avoidance of complications in this area requires familiarity with the variations that occur with respect to the ICA. The lateral sphenoid wall usually demonstrates an inward bulge harboring the ICA occasionally associated with the optic nerve lying superior to it. Kennedy et al noted that in 22% of 188 sphenoid sinuses examined, there was dehiscence of the bony canal over the ICA. In three cases, the artery was found to be completely dehiscent in the posterior wall of the posteriormost ethmoids. Near-midline ICA’s were seen in one case. It is believed that these anomalies account for the reported cases of ICA injury. These reports led to the development of the carotid drill by Sofferman.

In the event of carotid artery injury with massive hemorrhage, nasal packing should be placed immediately with manual compression of the ipsilateral cervical ICA. Controlled hypotension, blood products and neurosurgical and neuroradiological consultation should be called. Carotid angiography should then be undertaken. If this should indicate a significant carotid injury, balloon occlusion is attempted with EEG surveillance. If no changes occur on EEG, then carotid artery ligation may be performed. If there is evidence of lateralization on EEG with occlusion, then the balloon should be deflated and the packing left in place. In the ICU, Swan-Ganz catheterization and hypervolemic therapy should be implemented to optimize cerebral perfusion. Once this has been attained, occlusion should be reattempted. If evidence of adequate collateralization is present, then the carotid may be ligated. If not, then the patient should continue to be observed, and an attempt at removal of packing in the operating room should be attempted at a later time.

CSF leak resulting from penetration of the skull base near the area of the ethmoids or the sphenoids occurs in approximately 1% of cases. Preservation of the middle turbinate as a landmark is of critical importance in preventing complications. One should always operate lateral to its origin, since medial dissection can violate the thinner and lower cribriform plate. Although thicker than the cribriform, the fovea ethmoidalis is still susceptible to fracturing, especially medially. Therefore, one should try to remain as close to the lamina papyracea as possible when approaching the frontal recess. Similarly, the middle turbinate is important in locating the sphenoid sinus posteriorly, as its anterior wall lies in a plane between the superior inferior turbinate and the lower aspect of the middle turbinate. On average, the sphenoid sinus lies 7 centimeters posterior to the nasal introitus. This wall is very thin and should not require excessive force to infracture. Undue resistance implies that basilar skull bone is being impinged upon and that landmarks need to be reidentified.

CSF leaks noted intra-operatively can be repaired primarily using either temporalis fascia, septal or turbinate mucosa or fascia lata. The graft is placed over the defect and tucked under the bony edges as seen here. Muscle is then placed over this followed by Gelfoam for support. Leaks of the sphenoid sinus have been managed by plugging the defect with fibrin glue and Gelfoam followed by Gelfoam obliteration of the sphenoidotomy. Delayed fistula can be managed with bedrest with or without a lumbar drain. If this fails to resolve within 2 to 3 weeks, exploration either endoscopically with flourescein, extranasally or intranasally, or via craniotomy may be necessary. The use of antibiotics as prophylaxis against CNS infection is controversial.

Orbital complications, including blindness and diplopia, occur via two mechanisms: direct injury to the optic nerve or extraocular muscles, which is rare; and retro-orbital hematoma. Injury to either the anterior or posterior ethmoidal arteries or penetration of the lamina papyracea can lead to trace edema, periorbital and lid ecchymosis, chemosis and minimal proptosis, and may progress to massive proptosis with temporary loss of vision. If this is not rapidly addressed by the surgeon, persistent elevation of intraocular pressure with compromise of venous outflow leads to retinal ischemia with resultant permanent blindness. Use of general anesthesia increases risk as the patient is no longer able to sense pain when the lamina or ethmoid roof is injured. The eyes should remain uncovered and checked routinely by the surgeon in order to assess proptosis early. One should remember that the lamina papyracea lies superior and lateral to the natural maxillary ostium. Of note, several studies have cited a significantly greater incidence of orbital complications on the left side. This reflects an alteration in how the right-handed surgeon perceives the location of the ethmoids. On the right, they lie directly posterior as one would expect. On the left, however, scope orientation alters the view giving the surgeon the impression that the lamina papyracea is more lateral when in actuality it is more medial. Gentle palpation of the eye while dissecting in the area allows one to identify the lamina prior to entering it. Exposure of orbital fat in and of itself is usually of no consequence. However, a careful inspection of the eye should be undertaken. If signs of orbital hematoma are present, the patient should be admitted and observed as delayed blindness up to 48 hours post-op have been documented. Orbital packs should be avoided as these may increase intraorbital pressure. Management of an intraoperative orbital hematoma entails immediate ophthalmologic consultation and institution of several methods aimed at reducing intraorbital pressure. Eye massage is effective in that it helps to redistribute intraocular and extraocular fluids. This maneuver is absolutely contraindicated in patients with a prior history of ophthalmic surgery including corneal, retinal, or glaucoma filtering surgery. Acetazolamide 500 mg. IV can reduce intraorbital pressure by decreasing aqueous humor production, however its onset of action is slow. Mannitol has a much quicker onset and acts by osmotically drawing fluid out of the orbital spaces. A dose of 1-2 GRAMS per kilogram given over 20-30 minutes is usually safe and effective. Miotics should be avoided as these interfere with pupillary responses and thereby confuse the clinical picture. The use of steroids for this condition is not clear. Currently, no studies have shown a therapeutic gain associated with their use. Should medical management fail, lateral canthotomy has proven effective in reducing intraorbital hypertension. Briefly, the technique entails releasing the lateral canthal structures, including the lateral canthal tendon, by placing a straight hemostat across the area followed by sharp division of these structures down to the periorbital fascia. If this is not effective, medial canthotomy via the Lynch external ethmoidectomy approach can be performed with satisfactory results. Postoperative monitoring with diuretics in consultation with ophthalmology is usually uneventful.

Nasolacrimal duct stenosis resulting from middle meatal antrostomy is uncommon. It is presumed that the nasolacrimal duct is injured more frequently, but few cases result in frank obstruction with epiphora. Regardless, a few points are worthy of mention. First, it should be remembered that the nasolacrimal duct lies only 3-6 millimeters anterior to the natural ostium of the maxillary sinus and that the antrostomy should be made no further forward than the anterior end of the middle turbinate. If hard bone is encountered anteriorly, this likely represents a natural bony septum separating the ostium from the canal, or the lacrimal duct canal itself and should not be violated. Cases of persistent epiphora can be managed with serial lacrimal probing. Formal dacryocystorhinostomy, either endoscopically or via the external approach or both can be performed if necessary. A combined approach is currently favored in which the lacrimal sac is cannulated with a light source and endoscopically, the area of the lacrimal sac is identified, stripped of its bony and mucosal covering, and marsupialized into the frontal recess.

Finally, synechiae usually results from fibrous scar band formation between the lateral nasal wall and the middle and/or inferior turbinates. Atraumatic technique and stenting in these areas have been shown to be useful, but invariably, reduced incidence of this outcome results from meticulous debridement postoperatively in the office. Partial middle turbinectomy has been implemented by several authors with mixed results.

Major complications in endoscopic sinus surgery are rare. However, when they do occur they can be catastrophic and it behooves the surgeon to identify these problems early before permanent deficits evolve. Practical knowledge of the anatomy, both normal and variant, is requisite. Prevention of complications based on technique and implementation of limited surgery based on extent of disease are well established. Management strategies aimed at minimizing or reversing adverse events exist and these should be familiar to the endoscopic sinus surgeon.

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